Emphysematous gastritis is a rare but commonly fatal disease of the gastric wall caused by infection with gas-forming organisms. The first case was reported in 1889 and was identified on autopsy by necrotic gastric tissue with gas blebs in the mucosal wall. Modern medical advancements have allowed greater diagnostic capability in these patients. However, this has not altered the prognosis, with 61% mortality reported from 1889 to 19901 and 55% mortality reported from 1990 to the present day.2 This is a rare disease entity with fewer than 50 cases reported in the English literature.

The stomach is normally well protected from infection due to its acidity and rich vascular supply; however, certain risk factors predispose patients to emphysematous gastritis by compromising the integrity of the mucosal wall or the patient's immune system. Ingestion of corrosives, alcohol abuse, recent abdominal surgery, diabetes mellitus, use of immunosuppressants, and dialysis are some of the most common risk factors in previously reported cases.1,2 Our patient had a history of alcohol abuse.

Patients usually present with gastrointestinal symptoms such as abdominal pain, bloating, nausea, and vomiting as well as systemic signs and symptoms of infection. The diagnosis is made by correlation of the clinical features with radiographic evidence of intramural gas, which may be present in small bubbles or large streaks and often demonstrates thickened gastric rugae due to active inflammation.3

While the rarity of the disease precludes systematic study of management, outcomes are best when the disease is promptly recognized and broad-spectrum antibiotics and aggressive supportive care are initiated early. Gram-positive, gram-negative, anaerobic, and fungal organisms have all been implicated in emphysematous gastritis; thus, broad coverage is indicated and should be continued regardless of culture results due to the possibility of intramural organisms that are not cultured from blood or gastric contents.1,4 Emergent surgery has not been shown to alter mortality and should be reserved for failed medical management, perforation, or the development of peritonitis. The development of strictures is a common late sequela of emphysematous gastritis and should be surgically repaired after the infection has completely resolved.1,3

The differential diagnosis includes gastric emphysema (which is the result of air entering the gastric wall secondary to a traumatic tear), pulmonary bleb rupture, and distal obstruction leading to increased intragastric pressure.1 In contrast to emphysematous gastritis, the patients with these other conditions do not have signs of infection or sepsis and have normal gastric mucosa. The clinical course is usually self-limiting and the patients rarely require any therapeutic intervention.

Our patient was treated with aggressive intravenous fluid resuscitation, intravenous proton pump inhibitors, and antibiotics consisting of cefepime, metronidazole, and fluconazole. Blood cultures were obtained only after initiation of antibiotics but were negative for aerobic, anaerobic, and fungal growth. Endoscopy was scheduled, but the patient left against medical advice 6 days after admission, before the procedure could be performed. At this time, the patient was hemodynamically stable with a normal white blood cell count, had unremarkable physical examination results, and was tolerating a regular diet.

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